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Xu, C

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Author's Publications: search.filters.isAuthorOfPublication.28b29e4c-5fe0-4fd8-b609-f081690b3f39

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    Two-orbital SU(N) magnetism with ultracold alkaline-earth atoms
    (Nature Publishing Group, 2010) Gorshkov, Alexey; Hermele, M.; Gurarie, V.; Xu, C; Julienne, P. S.; Ye, J.; Zoller, P.; Demler, Eugene; Lukin, Mikhail; Rey, A. M.
    Fermionic alkaline-earth atoms have unique properties that make them attractive candidates for the realization of atomic clocks and degenerate quantum gases. At the same time, they are attracting considerable theoretical attention in the context of quantum information processing. Here we demonstrate that when such atoms are loaded in optical lattices, they can be used as quantum simulators of unique many-body phenomena. In particular, we show that the decoupling of the nuclear spin from the electronic angular momentum can be used to implement many-body systems with an unprecedented degree of symmetry, characterized by the SU(N) group with N as large as 10. Moreover, the interplay of the nuclear spin with the electronic degree of freedom provided by a stable optically excited state should enable the study of physics governed by the spin–orbital interaction. Such systems may provide valuable insights into the physics of strongly correlated transition-metal oxides, heavy-fermion materials and spin-liquid phases.
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    Hypoxia Activates a Ca-Permeable Cation Conductance Sensitive to Carbon Monoxide and to GsMTx-4 in Human and Mouse Sickle Erythrocytes
    (Public Library of Science, 2010) Vandorpe, David; Xu, C; Shmukler, Boris; Otterbein, Leo; Trudel, Marie; Sachs, Frederick; Gottlieb, Philip A.; Brugnara, Carlo; Alper, Seth
    Background: Deoxygenation of sickle erythrocytes activates a cation permeability of unknown molecular identity (Psickle), leading to elevated intracellular [Ca2+] ([Ca2+]i) and subsequent activation of KCa 3.1. The resulting erythrocyte volume decrease elevates intracellular hemoglobin S (HbSS) concentration, accelerates deoxygenation-induced HbSS polymerization, and increases the likelihood of cell sickling. Deoxygenation-induced currents sharing some properties of Psickle have been recorded from sickle erythrocytes in whole cell configuration. Methodology/Principal Findings: We now show by cell-attached and nystatin-permeabilized patch clamp recording from sickle erythrocytes of mouse and human that deoxygenation reversibly activates a Ca2+- and cation-permeable conductance sensitive to inhibition by Grammastola spatulata mechanotoxin-4 (GsMTx-4; 1 µM), dipyridamole (100 µM), DIDS (100 µM), and carbon monoxide (25 ppm pretreatment). Deoxygenation also elevates sickle erythrocyte [Ca2+]i, in a manner similarly inhibited by GsMTx-4 and by carbon monoxide. Normal human and mouse erythrocytes do not exhibit these responses to deoxygenation. Deoxygenation-induced elevation of [Ca2+]i in mouse sickle erythrocytes did not require KCa3.1 activity. Conclusions/Significance: The electrophysiological and fluorimetric data provide compelling evidence in sickle erythrocytes of mouse and human for a deoxygenation-induced, reversible, Ca2+-permeable cation conductance blocked by inhibition of HbSS polymerization and by an inhibitor of strctch-activated cation channels. This cation permeability pathway is likely an important source of intracellular Ca2+ for pathologic activation of KCa3.1 in sickle erythrocytes. Blockade of this pathway represents a novel therapeutic approach for treatment of sickle disease.